In the previous post I offered proof that my current LSJL was working for my fingers(and reported anecdotal evidence of increasing my wingspan by a couple of inches without photographic evidence) but that the LSJL method for the legs was lacking.  So I’m revising the LSJL method to be more like what I’m doing for the fingers which I’ve gotten gotten results from.  With an emphasis on intensity rather than duration.  If anyone has any ideas on how to get a more intense clamp please suggest them.  This is only for people with closed growth plates, people with open growth plates should clamp similarly but much lighter as there is no need to try to use clamping to create a more favorable microenvironment for cartilage growth.

You want to clamp on the synovial joint between the tibia and femur.    Michael has suggested that you should load lower on the epiphysis rather than above.  However, I think loading the synovial joint is important.  The bone there is weaker and it’s easier to cause deformation of the synovial joint then it is the bone itself.  There might be stimulus from the synovial joint that stimulates neo-growth plate formation.  The synovial joint is connected to the growth plate area after all.  You want to clamp more on the femur than the tibia as the clamp will eventually slip to be closer to the middle.  You always want to start clamping more on the bigger bone so it slips to the middle.  If it slips to be clamping on one bone then restart.  Essentially:  Make sure you are clamping the synovial joint.

Now you want to use the Irwin Quick Grip(Irwin Industrial Tools 512QCN Next Generation 12-Inch Clamp and Spreader).  But any clamp that can generate enough pressure is sufficient as long as it avoids slipping.  Try to clamp as hard as possible.  Use both hands to get harder clamps.  Take breaks with the clamp still on and the pressure still applied and try to clamp harder.  This method is untested so I can not make any guarantees on the optimal pressure nor can I guarantee that you won’t suffer an injury.  Right now my goal is to generate enough pressure such that there’s a visual or feeling of increased blood flow.  The goal is to generate hydrostatic pressure to create a pro-chondrogenic microenvironment to encourage new growth plate formation.  With my fingers I could see visually increased blood flow and I could feel it.  The goal is to generate enough pressure in the synovial joint to encourage a pro-chondrogenic microenvironment.  Any clamping method that does that is sufficient.

Here’s another angle:

Me clamping between the tibia and talus:

Me clamping between the talus and calcaneus:

Please let me know if you have any questions.  I know people will want a video so I’ll work on that for Part III.

Michael: Here is what I would suggest. Get a 2nd clamp to clamp simultaneously for the knee area. We do have two hands, and the clamping area is on the legs. A easy position to get into. To get the frequency correct, squeeze both hands at the same time.

Fit the two clamps along side of each other, one on the angular part while the other is on the sides, which you suggest. Since load is just pressure (Force/area) to increase the load, we just get a 2nd clamp to double the amount. At this point, I would not suggest increasing the amount of force from one clamp, but put the clamps into series on the sides of the tibia.

Note:  This post will provide evidence that LSJL does not merely expand the synovial joints but directly lengthens the bone.

I provided what I consider to be fairly irrefutable proof that I’ve increased finger length.  The issue is that finger length doesn’t come into play in athletics that much.  Larger hands could help in places where increased surface area would come into play.  I also increased wingspan which is more helpful in athletics but I have no documentation and wingspan isn’t measured by doctors.

So I have to return to developing a better methodology for LSJL for the legs which would increase height which is measured by doctors and important in everything in contrast to more niche uses for finger length and wingspan.  Here’s some of the methods I’ve tried.   I got initial results but stopped over time.  One of the reasons could have been that the results were due to dumbell loading since I stopped doing dumbell loading over time but I doubt that the results were due to dumbell loading since 65lbs is so slow.  There might be some sort of adaptive mechanism that reduces effectiveness over time.

The question is:  Why am I gaining length in my finger and arms but not in my legs?

The answer may be related to angular loading.  When I clamp a bone it begins to bend at an angle. Before I was trying to keep it straight which resulted in the knee popping out in the clamp at the top.  By allowing the knee to tilt the knee becomes trapped within the clamp stopping it from popping out.  My finger and other arm joints always tilt when I’m clamping them and I gained length there so it makes that I can allow for the knee joint to tilt and still gain length in that region.

I’m using the block to increase surface area.  I have to constantly adjust the block and clamp though for keeping it from slipping.  Slipping is far more an issue for leg clamping still so there are further advancements to be made here.

After trying this method for a couple of weeks it was too inconsistent.  Sometimes I would get a really good clamp and generate a lot of pressure other times the clamp would slip off before decent pressure was generated.  So right now I’m using the Irwin Quick Grip and I’ll cover what I’m doing in part II.  But right now I’m mainly focusing on one intense clamp rather than a certain time duration as before but bearing in mind to avoid injury which is possible since I am using so much force when clamping.  Although the time duration method was working with fingers/wing span, I think maximizing intensity is working even better even for fingers/arms.

I got a better angle of the finger length comparison.  I am only clamping my right finger and not my left.  You can clearly see that the right finger is definitively longer than the left.  It’s longer than it appears in the picture because I wanted to make sure the right knuckle was higher than the left so people didn’t think I was just sliding the right finger down.

Here’s another angle:

In this one it’s harder to prove that there’s no manipulation to alter finger length but it’s still another perspective.  You can also see the osteophyte on my right finger.  I studied a little bit about osteoarthritis and although osteophytes are a symptom of osteoarthritis they can be caused by other forms of mechanical stimuli too.  So, just because I have osteophytes doesn’t mean I have osteoarthritis.

Now to prove that it’s not just enlarged joints and it’s actually the bone that’s longer.

Comparison of two bones in the finger only and clearly the right finger bone is longer.  So LSJL lengthens bones and does not just merely expand the synovial joint.

Now here’s a thumb comparison.  I’ve only been doing LSJL on my left thumb and not my right.  I figured it would be unlikely for someone to argue that my right hand has always had longer figures if my right index finger was longer then the left but my left thumb was longer than my right.

And it looks like the left thumb is longer but I can’t rule out measurement error since it’s hard to tell exactly when the thumb ends on the hand.

I have before pictures of each appendage but it’s much easier to compare side to side against the contralateral limb.

So here’s some more evidence of LSJL but hopefully also switching up the knee and ankle method will be able to prove LSJL there and that is the big ticket for proof.  So look for Part II soon that explains the current LSJL technique I’m using(I have pretty much finalized the technique but need to take the pictures) and hopefully more LSJL proof.

Michael: I answered your later posts before this one, so I did not realize you accounted for synovial joint expansion.  As for the one question you wanted answered, I will just go back to the fact that the fingers and the arms are not always being pushed upon. With the legs, since we are always walking, the effects of the clamping might be negated by the loading from just walking itself.

As for the osteophyte issue, it is a unique sign that something is not going correctly. Has osteophytes also developed in the finger bone segments which were not clamped?

This supplement is available for sale and it seems to be promising for those who have existing growth plates:

Effects of Eucommia ulmoides Extract on Longitudinal Bone Growth Rate in Adolescent Female Rats.

Full study -> eucommia

“[We] investigate the effects of E. ulmoides extract on longitudinal bone growth rate, growth plate height, and the expressions of bone morphogenetic protein 2 (BMP-2) and insulin-like growth factor 1 (IGF-1) in adolescent female rats. In two groups, we administered a twice-daily dosage of E. ulmoides extract (at 30 and 100 mg/kg, respectively) per os over 4 days, and in a control group, we administered vehicle only under the same conditions. Longitudinal bone growth rate in newly synthesized bone was observed using tetracycline labeling. Chondrocyte proliferation in the growth plate was observed using cresyl violet dye. In addition, we analyzed the expressions of BMP-2 and IGF-1 using immunohistochemistry. Eucommia ulmoides extract significantly increased longitudinal bone growth rate and growth plate height in adolescent female rats. In the immunohistochemical study, E. ulmoides markedly increased BMP-2 and IGF-1 expressions in the proliferative and hypertrophic zones. In conclusion, E. ulmoides increased longitudinal bone growth rate by promoting chondrogenesis in the growth plate and the levels of BMP-2 and IGF-1. Eucommia ulmoides could be helpful for increasing bone growth in children who have growth retardation.”

“Because components in E. ulmoides extract activate osteoblast differentiation, we hypothesized that treatment with E. ulmoides extract would increase longitudinal bone growth rate.”<-Interesting considering it’s the growth plaate that increases height.

If you look at figure 2 in the full study, the growth plate looks bigger but it doesn’t have the dramatic differences that other chemicals or methods induce in the growth plate.  Which means that the risk is that this chemical only increases growth rate and not adult height.  According to Table 1, this compound increased levels of BMP-2 and IGF-1 by up to 50% in the resting, proliferative, and hypertrophic zone.

“At the dose of 100 mg/kg, E. ulmoides caused a significant acceleration of longitudinal bone growth rate, which was 373.1 ± 24.4 µm/day (6.4%) compared with the control group, which was 350.8 ± 18.5 µm/day. At the dose of 30 mg/kg, E. ulmoides caused an acceleration of longitudinal bone growth rate of 360.5 ± 23.5 µm/day (2.8%) compared with the control group.”

I wrote more about Cilia and the growth plate here.  By understanding the growth plate response of load we can understand how LSJL influences growth plate development and how crucial it is to have a growth plate in place for LSJL to work.  This study provides evidence that the adaptation to LSJL is atypical to normal load on the growth plate.

The growth plate’s response to load is partially mediated by mechano-sensing via the chondrocytic primary cilium.

Growth Plate Cilia<-link to pdf

“Chondrocytes sense and respond to mechanical stimulation. The primary cilium has been identified as a mechano-sensor in several cell types, including renal epithelial cells and endothelium, and accumulating evidence connects it to mechano-transduction in chondrocytes. In the growth plate, the primary cilium is involved in several regulatory pathways, such as the non-canonical Wnt and Indian Hedgehog.  It mediates cell shape, orientation, growth, and differentiation in the growth plate. Mechanical load enhances ciliogenesis in the growth plate. This leads to alterations in the expression and localization of key members of the Ihh-PTHrP loop resulting in decreased proliferation and an abnormal switch from proliferation to differentiation, together with abnormal chondrocyte morphology and organization. We use the chondrogenic cell line ATDC5, a model for growth-plate chondrocytes, to understand the mechanisms mediating the participation of the primary cilium, and in particular KIF3A, in the cell’s response to mechanical stimulation. This key component of the cilium mediates gene expression in response to mechanical stimulation.”

“The primary cilium is critical to skeletal development; the embryonic cilium plays a role in the earliest cellular determinative events establishing left–right axis asymmetry and primary cilia in the early mesenchyme is necessary for proper anterior-posterior limb patterning”

“the primary cilium is required for bone cell response (increase in the expression of osteopontin) to dynamic fluid flow”

“The primary cilium mediates cell shape, orientation, growth, and differentiation in the growth plate as deletion of KIF3A, a subunit of the motor protein kinesin-II, results in defects in the columnar organization of the growth plate together with reduced cell division, accelerated hypertrophic differentiation, and disruption of cell shape and orientation relative to the long axis of the bone”

“Ihh, directly through its receptor Patched-1 (ptc1), increases chondrocyte proliferation and inhibits its hypertrophic differentiation through induction of Parathyroid hormonerelated
protein (PTHrP) expression”

For mechanical stimulation, cells were stetched at 1HZ by 20% elongation.

“the transition between the proliferative zone (positive for collagen II) and hypertrophic zone (positive for collagen X) was more homogeneous in the growth plates that were subjected to loading, suggesting that not only proliferation is altered by the load, but also the switch between proliferation and differentiation is altered.”<-Thus suggesting that PTH and IHH was involved.  However, this was not the case with LSJL growth plates. In that study, the hypertrophic and proliferative zone was less homogeneous.

“[In loaded growth plates], cells in the proliferative zone deviated less from the center of the column compared with the control growth plates in which more cells deviated from the column line”

“Morphometric analysis showed a significant increase in the number of cells per defined area and a decrease in the average cell area”<-Both number of cells and cell area increased during LSJL loading.

“the cells in the proliferative zone were more spread out, whereas those in the hypertrophic zone were more spherical, suggesting that mechanical load affects chondrocyte morphology and organization within the growth plate.”

A diagram depecting a chondrocytes response to stress:

“a Unstimulated GP chondrocyte: Ihh, directly through its receptor Patched-1 (ptc1), located in the cilium, increases chondrocyte proliferation and inhibits its hypertrophic differentiation through induction of Parathyroid hormone-related protein (PTHrP) expression.  b Mechanical stimulated GP chondrocyte: morphological change of the cell together with up-regulation of cilia related genes (IFT88, KIF3A, PKD1 and PKD2) and formation of stress fibers.  Decrease in the expression of Ihh and ptc1 results in major decrease of PTHrP expression following reduced proliferation and switch for differentiation”

“we did not observe any significant difference in the cilia length caused by the mechanical stimulation.  In all checked samples, around 80 % of the cells presented cilia (counted according to acetylated-tubulin staining in comparison to nucleus DAPI staining), and cilia length was 2.4 lM,”

“primary articular chondrocytes [were subjected] to cyclic tensile strain up to 20 % for 1 h at 0.33 Hz and primary cilia prevalence was not altered in response to this stimulation”  However other studies found that cilia subjected to higher strain were reduced by 15.1%.

In this study C-Fos and egr1 were upregulated two genes that were also upregulated by LSJL.

“tensile load is induced during stretching while compression load is induced during release from stretch. Both acts induce fluid flow, thus creating shear load.”

“in control cells, mechanical stimulation induced Ihh expression, and activation of the pathway by SAG stimulation increased the expression of ptc1 and its accumulation in the cilium. Knockdown of KIF3A abolished these responses.”

osteosclerosis <-the pdf.  Osteosclerosis is increased bone density.

Osteosclerosis induced by denosumab

“A 10-year-old boy, 144 cm tall, was referred to our hospital in October, 2012, with a 2 month history of persistent pain in the buttocks. He had altered gait due to pain, but no disturbance of bladder or bowels. Radiographs, CT, and MRI showed a large osteolytic lesion in the sacrum, and examination of a bone biopsy sample confirmed a giant cell tumour of bone, which we considered to be unresectable because of the potential risk of neurological deficit and massive bleeding. We obtained informed consent from the patient and his parents and the review board for off-label use of denosumab, a potent inhibitor of osteoclastic bone resorption, to reduce the tumour mass. We gave subcutaneous denosumab 120 mg every 4 weeks, with loading doses on days 8 and 15 of the first cycle. Due to the excellent clinical response and the obvious sclerotic changes along the growth plates (figure) we stopped treatment after five cycles (seven injections). The sclerosing bands were seen in almost all the radiographs of metaphyses, most prominently in the distal radius and ulna, and also in the proximal humerus, proximal femur, and phalanges of the fingers. During the 5 months off treatment the tumour grew again, so we restarted treatment with denosumab for 4 months until the tumour had reduced enough in size for surgery to be safely carried out. Before surgery repeat radiographs showed double-layered sclerotic bands at the metaphysis (figure), reflecting the longitudinal bone growth during the periods on and off denosumab. At last follow-up in March, 2014, the patient showed no signs of growth retardation (151 cm tall), was able to participate in sports without pain, and showed no evidence of tumour recurrence.”

“(A) Plain radiograph of the right wrist before denosumab. (B) Metaphyseal sclerotic bands in the distal radius and ulna after five cycles of treatment. (C) Double-layered sclerotic bands (arrows) after two courses of denosumab with an interval between the treatment.”

The growth plates seem to be longer after osteoclasts have been inhibited but note that taller growth plates doesn’t always lead to increased height.

Growth retardation assessment was done after two years so permanent alterations will have to be longer.

ijmm_36_2_571_PDFCysteine induces longitudinal bone growth in mice by upregulating IGF-I.

“Cysteine (Cys) is known to exert various effects, such as antioxidant, antipancreatitic and antidiabetic effects. However, the effects of Cys on longitudinal bone growth have not been elucidate to date. Thus, the aim of the present study was to evaluate the effects of Cys on bone growth. Growth‑plate thickness and bone parameters, such as bone volume/tissue volume (BV/TV), trabecular thickness (Tb.Th), trabecular number (Tb.N), connectivity density (Conn.D) and total porosity were analyzed by means of micro-computed tomography (µCT). The levels of serum insulin‑like growth factor‑I (IGF‑I) were measured by enzyme‑linked immunosorbent assay (ELISA). Hepatic IGF‑I mRNA expression was analyzed by quantitative polymerase chain reaction (qPCR). The phosphorylation of Janus kinase 2 (JAK2) and signal transducer and activator of transcription 5 (STAT5) was investigated by western blot analysis. Our results revealed that Cys increased IGF‑I mRNA expression in HepG2 cells. The thickness of the growth plates was increased following treatment with Cys. Moreover, BV/TV, Tb.Th, TbN, Conn.D and total porosity were improved following treatment with Cys. Hepatic IGF‑I mRNA expression and serum IGF‑I levels were increased by Cys. The levels of phosphorylated JAK2 and STAT5 were elevated by Cys. The findings of our study indicate that Cys increases the thickness of growth plates through the upregulation of IGF‑I, which results from the phosphorylation of JAK2-STAT5. Thus, our data suggest that Cys may have potential for use as a growth-promoting agent.”

Cysteine is found in dietary sources but it may be possible to be deficient.

“Treatment with 50 mg/ml of Cys had the most prominent effect, and thus we evaluated the effects of treatment with 50 mg/kg of Cys in the next set of experiments, i.e., in vivo mouse models.”

“The thickness of the growth plates in the proximal tibias in the CON and PEM{protein deficient group} groups were 124.0±2.9 and 90.1±3.1, respectively; the growth-plate thickness in the Cys group was 117.0±4.3″<-Cysteine did not increase growth plate thickness versus control group.

“the levels of p-JAK2 and p-STAT5 in the liver were decreased due to malnutrition. However, the decrease in the levels of p-JAK2 and p-STAT5 was reversed by treatment with Cys”

“In general, endochondral cell proliferation in the growth plate results in bone growth. Thus, growth-plate thickness is a direct indicator of linear bone growth”